Combined endovascular embolization and surgery in the management of cerebral arteriovenous malformations: experience with 101 cases

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✓ The authors describe their experience with 101 cerebral arteriovenous malformations (AVM's) treated by endovascular embolization followed by surgical removal. Fifty-three patients presented with intracranial hemorrhage and 35 had seizures. Based on the classification of Spetzler and Martin, two AVM's were Grade I, 13 were Grade II, 26 were Grade III, 43 were Grade IV, and 17 were Grade V, Fifty-six AVM's were in the right hemisphere, 28 were in the left hemisphere, 12 were in the corpus callosum, and five involved the cerebellum. In 50 cases, presurgical obliteration of 50% to 75% of the AVM nidus was achieved by embolization, and in 31 cases this percentage increased to between 75% and 90%. In 97 (96%) patients, complete surgical removal of the AVM was obtained.

Morbidity resulting from preoperative endovascular embolization was classified as mild in 3.9% of the cases, moderate in 6.9%, and severe in 1.98%. The death rate related to embolization was 0.9%. The immediate postsurgical morbidity was classified as mild in 5.9% of the cases, moderate in 10.8%, and severe in 5.9%. The overall long-term morbidity was mild in 5.9% of the cases, moderate in 6.9%, and severe in 1.98%. Two patients (1.98%) died due to intractable intraoperative hemorrhage and two (1.98%) as a result of postsurgical pulmonary complications.

Article Information

Address for Dr. Dion: University of Virginia, Charlottesville, Virginia.Address for Dr. Lylyk: Instituto de Investigaciones Neurologicas Raul Carrea, ENERI-Neurosurgery, 2039 Billinghurst-PBA, Buenas Aires, Argentina.Address for Drs. Fox, Pelz, Drake, and Girvin: University of Western Ontario, London, Ontario, Canada.Address for Dr. Debrun: Johns Hopkins Hospital, Baltimore, Maryland.Address reprint requests to: Fernando Viñuela, M.D., Service of Endovascular Therapy, University of California School of Medicine, 10833 Le Conte Avenue, Los Angeles, California 90024.

© AANS, except where prohibited by US copyright law.

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Figures

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    Pre- and postembolization intravascular pressure monitoring. Left: Pre-embolization superselective angiogram of a posterior parietal feeder. Note the microcatheter tip (arrowhead), a normal cortical artery (black arrow), and three arteriovenous malformation (AVM) feeders (open arrows). The mean pressure is 108 mm Hg in the internal carotid artery (ICA) and 54 mm Hg in the AVM feeder. Right: Postembolization superselective angiogram showing obliteration of AVM feeders while sparing the normal cortical artery (black arrows). The mean pressure in the AVM feeder increased 10 mm Hg to 64 mm Hg, while the mean pressure in the ICA dropped 10 mm Hg to 98 mm Hg. Open arrow indicates the tip of the microcatheter.

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    Primary arteriovenous malformation (AVM) feeder versus feeder en passage. Left: Superselective angiogram of a left posterior temporal primary feeder. Note the microcatheter tip (arrowhead), the arterial feeder (open arrow) supplying only the AVM nidus (long arrow), and the draining vein (short arrow). Right: Superselective arteriogram of a distal middle cerebral artery showing an example of a feeder en passage. Note the microcatheter tip (arrowhead) within the distal sylvian fissure and the angular artery supplying the AVM nidus (open arrow) and the distal normal brain (long arrow), a feeder en passage.

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    Changes in the surgical field after embolization. Left: Surgical field of a large nonembolized cortical arteriovenous malformation (AVM). Note the marked engorgement of cortical draining veins and the array of subpial collateral vessels in the surrounding brain. Right: Surgical field 12 days postembolization. There is thrombosis of cortical veins (arrows) that drained embolized portions of the AVM nidus. The surrounding brain is not edematous and there are relatively few subpial collateral vessels. This type of result is obtained only when a substantial portion of the AVM nidus is occluded by embolization.

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    Shift of functional cortex and brain arteriovenous malformation (AVM). Left: Lateral left internal carotid angiogram showing an AVM involving the superior and middle temporal gyri in the left dominant hemisphere. A posterior temporal feeder (open arrow) was catheterized using a Tracker microcatheter. Center: Superselective angiogram of the posterior temporal feeder showing the microcatheter (arrowheads) and the column of contrast material opacifying a feeder en passage with several twigs (small arrows) supplying the AVM nidus. The injection of 30 mg Amytal elicited abnormalities on electroencephalography but no clinical speech abnormalities. Open arrow indicates the AVM in the superior temporal gyrus. Right: Intraoperative electrocorticography in an awake patient showing shift of language cortex toward the posterior parietal region (arrow). Complete surgical resection of the AVM was achieved, resulting in temporary mild dysphasia.

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    Presurgical embolization of a large cortical arteriovenous malformation (AVM). A: Early arterial phase of the lateral internal carotid angiogram showing a large parietal AVM supplied by posterior cerebral (square open arrow), middle cerebral (straight arrows), and anterior cerebral (tailed arrow) feeders. B: Late arterial phase of the lateral internal carotid angiogram. C: Superselective right posterior cerebral arteriogram showing the microcatheter (open arrows) selectively positioned in a temporoparietal feeder (straight arrow). Note the portion of the AVM nidus (curved solid arrow) and corresponding cortical draining vein (curved open arrow). This feeder was embolized with isobutyl 2-cyanoacrylate (IBCA). D: Superselective pericallosal angiogram showing an arterial feeder (tailed arrow), the AVM nidus (open arrow), and a draining vein (curved arrow). The white material posterior to the AVM nidus is radiopaque IBCA delivered through the posterior cerebral artery feeders. A similar technique was used to embolize the anterior cerebral and middle cerebral artery feeders. E: Right internal carotid angiogram obtained immediately postembolization showing occlusion of a large portion of the AVM nidus. Complete uneventful surgical resection of the residual AVM was performed 10 days after embolization.

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